Tumor necrosis factor (TNF) enhances leukocyte adherence to vascular endothelium and increases procoagulant activity in the endothelial cells. Thus it may be implicated in the pathogenesis of acute vascular occlusions. To study the role of TNF in the early stages of acute myocardial infarction (MI), the authors measured circulating TNF levels in the sera of patients with acute MI and unstable angina pectoris. Blood samples were obtained within six hours after onset of chest pain and stored at -70 degrees until tested. A sensitive sandwich enzyme-linked immunosorbent assay (ELISA) test was used for TNF measurement. C-reactive protein (CRP) levels were determined semiquantitatively. Immediate complications such as heart failure, arrhythmia, and shock were also noted. Twenty-four patients with electrocardiographically and biochemically confirmed acute MI and 14 patients with unstable angina pectoris were included in the study. TNF levels were serially assessed at the time of admission and at hours 6, 24, 48, 72, and 96 after onset of chest pain in 2 patients with acute MI. Detectable TNF was found in 13 sera of the acute MI group (range; 10-1510 pg/mL) and 4 sera of the angina pectoris group (range; 15-240 pg/mL). There was no correlation between the serum TNF levels and the occurrence of complications and the extent of myocardial damage. CRP response was unrelated to TNF levels. Contrary to previous reports, serial measurement of TNF revealed that peak values were reached within six hours and disappeared after twenty-four hours.(ABSTRACT TRUNCATED AT 250 WORDS)

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Masked hypertension (MHT) is a popular entity with increased risk of developing sustained hypertension, heart attack, stroke, and death. Subjects have normal blood pressure (BP) at office but elevated values at night so it is difficult to diagnose. Exaggerated blood pressure response to exercise (EBPR) is also a predictor of future hypertension. To investigate the relationship between these two entities, we evaluated 61 normotensive subjects with EBPR. The subjects underwent 24-h ambulatory blood pressure monitoring (ABPM). The prevalence of masked hypertension among subjects with EBPR was 41%. Body mass index (BMI), non-high density lipoprotein (HDL) cholesterol, diastolic blood pressure (DBP) at peak exercise and recovery, nondipping DBP pattern, and elevated early morning average BPs were associated with masked hypertension. In multivariate logistic regression analysis, the DBP measured at peak exercise was detected as an independent predictor of MHT in subjects with EBPR. Subjects with abnormally elevated BP during exercise are prone to MHT, necessitate medical assessment and close follow-up for hypertension.

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Circ J 2009; 73: 899 -904 lood pressure (BP) shows diurnal variation, reaching the highest level during the morning and then declining to reach a trough value at about midnight. In the early morning, an abrupt and steep acceleration in BP occurs, coincident with arousal and arising from overnight sleep. 1 However, there is considerable variation in the diurnal rhythm of BP in different individuals.In several studies of hypertensives, it has been shown that several abnormalities in BP circadian rhythm such as nondipping status (NDS), increased morning BP (MBP) and increased MBP surge (MBPS) have an association with cardiovascular (CV) target organ damage (TOD). [2][3][4][5] In normotensives, the relation between the abnormalities in BP circadian rhythm and TOD has not been examined sufficiently. 6,7 Therefore, in the present study, we have attempted to determine each effect of these abnormalities on TOD separately and to determine which abnormality in BP circadian rhythm (NDS, increased MBP or increased MBPS) is more closely related to TOD in normotensives. MethodsBetween December 2005 and December 2007, among the normotensives applying at the Cardiology Clinic of Meram Medical Faculty of Selcuk University who did not exhibit any significant cardiac pathology, 47 dipper subjects (28 women, mean age 45.8±9.3 years) and 32 non-dipper subjects (25 women, mean age 49.1±8.3 years) were included in the present study according to following criteria: (1) office BP <140/90 mmHg; and (2) average 24-h ambulatory BP <130/80 mmHg. 8 None of the subjects selected took antihypertensive medication or had a history of hypertension. Subjects with renal dysfunction (serum creatinine ≥2 mg/dl or macroalbuminuria >300 mg/24 h), hepatic failure, a history of coronary artery disease, stroke, heart failure, arrhythmia, diabetes mellitus, and/or those currently smoking were excluded. Those not smoking for at least last 2 years were accepted to be non-smokers. Subjects who reported in our post-ABPM questionnaire that their sleep was severely disturbed when wearing the ABPM were also excluded. Each was adequately informed about the aim of the present study before he/she was accepted to be enrolled.Office BP was measured using a calibrated mercury sphygmomanometer in an office setting after the subjects had rested at least 5 min in a seated position. Three measurements were taken at 2-min intervals, and the average of these measurements was used to define office systolic BP (SBP) and diastolic BP (DBP). Dyslipidemia was defined by a total cholesterol level >240 mg/dl or taking lipid-lowering agents. Body mass index (BMI) was calculated as weight (kg)/height (m) 2 . The body surface area was calculated according to the following formula in square meters: 0.007184 × weight (kg) 0.425 × height (cm) 0.725 . (Received October 6, 2008; revised manuscript received November 30, 2008; accepted December 25, 2008; released online March 18, 2009